Loss of Body Cell Mass in Cushing’s Syndrome: Effect of Treatment

Abstract

Cushing's syndrome (CS) is associated with low fat-free mass, but it is unclear whether hypercortisolism causes a loss of whole body protein. Body composition was studied prospectively in 15 patients with untreated CS (n = 14 pituitary adenoma; n = 1 adrenal adenoma), in 15 nonobese healthy controls, and in 15 weight-matched obese controls by 3 different methods: total body potassium counting (TBP), bioelectrical impedance analysis (BIA), and anthropometry. In 6 patients, body composition was studied before and within 6 months after pituitary surgery. In CS patients and weight-matched controls, body weight and total body fat were significantly higher than in nonobese controls. In CS patients, TBP was 18.4% lower than predicted, whereas in weight-matched controls TBP was 7.1% higher than predicted. As compared with nonobese and weight-matched controls, in CS patients TBP indicated a significant loss of body cell mass (BCM) of -20.2 and -21.1%, respectively. A significantly reduced arm muscle area of -21.3% compared with weight-matched controls also indicated a loss of whole body protein. In CS, however, BIA overestimated BCM when compared with TBP by +18% and agreement between BIA and TBP in the individual patient was poor (limits of agreement plus minus 27.6%), indicating the invalidity of standard BIA equations in this population. Measurements performed before and 6 months after successful pituitary surgery demonstrated a significant loss of body weight (-11%) and body fat (-33%), but BCM and muscle mass remained on a constant low level. In conclusion, this study shows that, in patients with CS, a significantly reduced BCM indicates a true protein loss. The second interesting finding is that in the early recovery after successful treatment of hypercortisolism patients lose body fat without gaining BCM or muscle mass.

Body composition and bone mineral density in women with Cushing's syndrome in remission and the association with common genetic variants influencing glucocorticoid sensitivity

“…Our results also indicate that the central obesity associated with long-term hypercortisolism in CS is not completely reversible after treatment. Previous studies on the reversibility of reduced LBM and skeletal muscle mass have demonstrated either unchanged (4,8,9,10) or reduced LBM after treatment (7,11). In our study, after adjustment for various confounders, no difference in skeletal muscle mass was observed between patients and controls.…”

“…The study also demonstrates that ongoing GC replacement and a common polymorphism in the GC receptor gene are associated with adverse skeletal health in patients with CS in long-term remission. Adipose tissue mass decreases after treatment for CS (4,7,8,9,10), but whether complete normalisation occurs at long-term follow-up is not fully explored. One previous cross-sectional study found an increased total and abdominal fat mass in patients with CS after a mean time of 11 years in remission in comparison with age-, gender-and BMI-matched controls (11).…”

Metabolic comorbidities in Cushing's syndrome

“…Muscle damage can persist both short-and long-term after cure. Indeed, the reduced muscle area in the arms showed no relevant improvement 6 months after successful treatment (102). MRI body composition assessment of CD patients 20 months after remission showed that total and limb skeletal muscle is actually reduced compared to active disease (99).…”

Effects of Cortisol on Carbohydrate, Lipid, and Protein Metabolism: Studies of Acute Cortisol Withdrawal in Adrenocortical Failure

“…Thus, when in excess, cortisol is an overall catabolic hormone, which decreases lean body mass and muscle mass and may increase energy expenditure (7). At the same time, glucocorticoids increase appetite and food intake (7) and may increase fat mass (8,9). Cortisol also induces insulin resistance (2,3), and it has been proposed that glucocorticoids could contribute to the metabolic syndrome and cardiovascular disease (10,11).…”